EHR519 2024 Week 12a COPD Pathophysiology, Medications, & Considerations PDF

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Warning This material has been produced and communicated to you by or on behalf of Charles Sturt University in accordance with section 113P of the copyright act (Act). The material in this communication may by subject to copyright under the act. Any further reproduction or communication of this material by you may be the subject of copyright protection under this act. Do not remove this notice  Pathophysiology, considerations and medications for COPD EHR519 Week 12a Learning Outcomes be able to explain the pathophysiology of pulmonary conditions as it relates to exercise physiology; be able to outline the risk factors, complications and co-morbidities that must be accounted for when applying exercise interventions to individuals with pulmonary conditions; be able to describe the effects of commonly prescribed medications on acute and chronic exercise responses that must be accounted for when applying exercise interventions to individuals with pulmonary conditions; be able to explain the diagnostic techniques and treatment procedures used in the treatment of pulmonary conditions; Week Overview 1. Pathophysiology 2. Common medications 3. Considerations for exercise testing and prescription COPD 5  Chronic Obstructive Pulmonary Disorder (COPD) “heterogeneous lung condition characterised by chronic respiratory symptoms (dyspnea, cough, sputum production and/or exacerbations) due to abnormalities of the airways (bronchitis, bronchiolitis) and/or alveoli (emphysema) that cause persistent, often progressive, airflow obstruction” (GOLD report 2023) Global Initiative for Chronic Obstructive Lung Disease (GOLD) outlines major risk factors: Exposure to noxious particles or gases from cigarettes or other types of tobacco, marijuana, environmental tobacco smoke, occupational exposures and air pollution Genetic syndromes Abnormal lung development Oxidative stress-induced accelerated ageing 6  Clinical presentation and Diagnostic criteria Typical COPD = dyspnoea, wheezing, chest tightness, fatigue, activity limitation, and/or cough with or without sputum production. May experience acute events of increased respiratory symptoms (exacerbations) that require specific preventive and therapeutic measures. Those with COPD often have other comorbid diseases that can mimic and/or aggravate an acute exacerbation. (requiring specific treatment) Diagnosis = the presence of non-fully reversible airflow limitation (FEV1/FVC < 0.7 post- bronchodilation) measured by spirometry However, some have structural lung lesions (e.g., emphysema) and/or physiological abnormalities (low-normal FEV1, gas trapping, hyperinflation) with an FEV1/FVC ratio ≥ 0.7 post-bronchodilation These are classed as having ‘Pre-COPD’. The term ‘PRISm’ (Preserved Ratio Impaired Spirometry) has been proposed to identify those with normal ratio but abnormal spirometry. Pre-COPD or PRISm = increased risk of developing COPD, but not all of them do. 7 Aetiology, pathobiology & pathology of COPD leading to airflow limitation & clinical manifestations  COPD Mechanisms are related to Structural abnormalities at the small airways (i.e. obstructive bronchiolitis) Pulmonary parenchyma (i.e emphysema) Chronic bronchitis: presence of chronic productive cough on most days for a period of at least 3 consecutive months in each of 2 successive years. Cough is related of mucus hypersecretion Emphysema: pathological or anatomical diagnosis due to abnormal permanent enlargement of the respiratory bronchioles and alveoli, air spaces distal to the terminal bronchioles Accompanied by destruction of lung parenchyma without fibrosis 9  Clients with COPD may experience periods of exacerbation and worsening symptoms Often require hospitalisation Supplemental therapies including bronchodilators, antibiotics, oxygen therapy, ventilator support, mechanical ventilation. Exacerbations can lead to: Reduced QaL Increased pulmonary function decline Prolonged recovery times Increased mortality Most clients with COPD do not experience the significant reversibility/symptom-free periods compared to clients with asthma 10 COPD vs Asthma Chronic airway inflammation and hyper-responsiveness of the tracheobronchial tree Due to stimuli Unlike COPD, experience exacerbations but they are interspersed with symptom-free periods According to GOLD, patients experiencing recurrent airflow obstruction with a combination of asthma and COPD features are diagnosed with asthma and COPD overlap syndrome 11 Factors that influence COPD progression Genetic factors Age >45yrs) and gender (> in women) Race (2.3 x higher in Indigenous) Lung growth and development Exposure to particles Socioeconomic status Asthma & airway hyper-reactivity Chronic bronchitis Infections 12  Pathology, pathogenesis and pathophysiology Pathology Chronic inflammation Structural changes Pathogenesis Oxidative stress Protease-antiprotease imbalance Inflammatory cells Inflammatory mediators Peribronchiolar and interstitial fibrosis Pathophysiology Airflow limitation and gas trapping Gas exchange abnormalities Mucus hypersecretion Pulmonary hypertension 13  Pathogenesis of COPD - Inflammation Inflammation is present in all areas of the lungs as a protective response to the inhaled toxins (smoking) Tissue destruction Impairment of defence mechanisms Disruption to repair mechanisms Smoking and associated inflammation contributed to an imbalance between oxidants and antioxidants, creating an environment of oxidative stress in the lung 14  Inflammatory markers and COPD Increased numbers of neutrophils, marcophages, T lymphocytes Typically reflects the degree of airflow obstruction Release of cytokines and mediators Leukotriene B4: a neutrophil and T cell chemoattractant which is produced by macrophages, neutrophils, and epithelial cells Chemotactic factors such as the CXC chemokines interleukin 8 and growth related oncogene α, which are produced by macrophages and epithelial cells. These attract cells from the circulation and amplify pro- inflammatory responses Pro-inflammatory cytokines such as TNF-α and IL-1 and 6 Growth factors such as transforming growth factor β, which may cause fibrosis in the airways either directly or through release of another cytokine, connective tissue growth factor. 15  Protease and anti-tease imbalance Protease: enzymes which break down proteins and peptides ↑ production (or activity) of proteases and inactivation of anti-proteases = imbalance. Cigarette smoke, and inflammation itself, produce oxidative stress, which primes several inflammatory cells to release a combination of proteases and inactivates several antiproteases by oxidation. 16  Oxidative Stress Sources of oxidants include cigarette smoke and reactive oxygen and nitrogen species released from inflammatory cells. This creates an imbalance in oxidants and antioxidants of oxidative stress. Markers of oxidative stress are increased in stable COPD and are further increased in exacerbations. Oxidative stress can lead to inactivation of antiproteases or stimulation of mucous production. It can also amplify inflammation by enhancing transcription factor activation (such as nuclear factor B) and hence gene expression of pro-inflammatory mediators. 17  Pathophysiology of COPD Given the effect tobacco has on the respiratory system, it is the primary risk factor for developing COPD Secondary effects on skeletal muscle Specially, sites which are affected Bronchi → enlarged mucus glands and dilated gland ducts Bronchioles → mucus plugging, inflammation, increased in airway smooth muscle tone which decrease airway cross-sectional area Greatest effect on airflow and spirometry results Pulmonary parenchyma and vasculature → Loss of alveoli wall support (tethering) which keep airways open during expiration; Diminished elastic recoil which reduces the force of airflow during expiration Increased work by respiratory muscles to meet ventilatory demands 18 Airflow obstruction and hyperinflation Main site of airflow obstruction occurs in the small conducting airways (